Roth E, Schulman S
Division of Hematology, Montefiore Hospital and the Albert Einstein College of Medicine, Bronx, New York 10467.
Br J Haematol. 1988 Nov;70(3):363-7. doi: 10.1111/j.1365-2141.1988.tb02495.x.
It has recently been found that growth of P. falciparum in human G6PD deficient red cells is impaired in vitro; however, the inhibition is overcome after two or three growth cycles. There is evidence to suggest that the parasite can produce its own G6PD enzyme which may compensate for the lack of host enzyme and could account for the resumption of normal growth in G6PD deficient host cells. It is unclear whether the parasite enzyme can enable the host cell to resist oxidative stress as normal cells do. To answer this question, P. falciparum was grown in vitro in: (a) normal red cells, (b) G6PD deficient red cells for one growth cycle only, (c) G6PD deficient cells for a minimum of five cycles. All groups were then challenged with acetylphenylhydrazine (APH) which served as an oxidative stress. Both G6PD (A-) and Mediterranean deficient types were studied. The results show a two-fold increase in resistance to oxidative stress by parasites adapted to G6PD-Mediterranean deficient host cells as compared to unadapted ones, but the parasite-red cell system remains 4 times more sensitive to APH than normal infected cells. In parasitized G6PD (A-) red cells, evidence of adaptation could be seen in the growth curves, but no detectable increase in resistance to APH was found in adapted parasites. It is concluded that the role of the parasite G6PD is not likely to be mainly related to oxidative stress resistance and therefore other functions of this enzyme should be investigated.
最近发现，恶性疟原虫在体外人葡萄糖-6-磷酸脱氢酶（G6PD）缺乏的红细胞中生长受到损害；然而，经过两到三个生长周期后，这种抑制作用会被克服。有证据表明，疟原虫能够产生自身的G6PD酶，该酶可能弥补宿主酶的缺乏，并可解释G6PD缺乏的宿主细胞中正常生长的恢复。尚不清楚疟原虫酶是否能使宿主细胞像正常细胞一样抵抗氧化应激。为了回答这个问题，恶性疟原虫在体外培养于：（a）正常红细胞，（b）仅经过一个生长周期的G6PD缺乏的红细胞，（c）至少经过五个周期的G6PD缺乏的细胞。然后所有组都用乙酰苯肼（APH）进行挑战，APH作为氧化应激源。对G6PD（A-）缺乏型和地中海缺乏型都进行了研究。结果显示，与未适应的疟原虫相比，适应G6PD地中海缺乏型宿主细胞的疟原虫对氧化应激的抵抗力增加了两倍，但疟原虫-红细胞系统对APH的敏感性仍比正常感染细胞高4倍。在寄生有疟原虫的G6PD（A-）红细胞中，在生长曲线中可以看到适应的迹象，但在适应的疟原虫中未发现对APH抵抗力的可检测增加。结论是，疟原虫G6PD的作用不太可能主要与氧化应激抵抗有关，因此应该研究这种酶的其他功能。
